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. 2015 Dec 30;33(4):328–336. doi: 10.3857/roj.2015.33.4.328

Fig. 3. S-allylcysteine (SAC) inhibited the activation of Met and downstream signaling by hepatocyte growth factor (HGF). (A) HONE1 or HNE1 cells were pretreated with 0, 10, 20, or 40 mM SAC for 2 hours followed by treatment with 10 ng/mL HGF for 10 minutes. The cells were then harvested and western blot analysis was performed for p-Met, Met, p-extracellular related kinase (p-ERK), ERK, p-focal adhesion kinase (p-FAK), FAK, p-Src, and Src (shock protein 60 was used as a loading control). (B) HONE1 or HNE1 cells were treated with HGF (10 ng/mL) alone, SAC (10, 20, or 40 mM) and HGF, or SAC alone (10, 20, or 40 mM) for 24 hours. The cells were then harvested and western blot analysis was performed for Slug, p-FAK, FAK, p-Src, and Src. (C) HONE1 or HNE1 cells were treated with HGF (10 ng/mL) alone, SAC (10, 20, or 40 mM) and HGF, or SAC alone (10, 20, or 40 mM) for 24 hours. The cells were then harvested and matrix metalloproteinase-2 (MMP2) and MMP9 activity was assessed by gelatin zymography.

Fig. 3